The aim of our study was to evaluate the fibrinolytic system in patients with retinal branch vein occlusion (RVO). The following tests were carried out: prothrombin time, partial thromboplastin time (PTT), fibrinogen degradation products, euglobulin lysis time, fibrinogen, pasminogen, antithrombin III, α2-antiplasmin and α2-macroglobulin. Comparing the results of patients with those of normal controls, only the fibrinogen increase and PTT shortening were significantly different. All other tests taken into account were within normal limits. Only the patients without other associated diseases (diabetes or hypertension) showed a significant activation of fibrinolysis (either with respect to normal or to other RVO patient groups). In conclusion, no important fibrinolytic impairment was seen in our longstanding RVO patients. Fibrinolytic activation seen in patients without verified associated diseases may be related to the presence of a sound endothelium, still able to release plasminogen activators in response to RVO. The fibrinogen and PTT changes in RVO were probably due to other associated diseases.
Hemorheological parameters (viscosity of whole blood, plasma viscosity, hematocrit, velocity of red blood cells) were studied in 30 patients with coronary artery disease (15 patients with acute myocardial infarction, 15 patients with chronic angina), 14 subjects at high risk for ischemic heart disease and 14 normal volunteers matched for sex and age. Viscosity of whole blood was high in all coronary disease patients and in high-risk subjects as compared with controls. Velocity of red blood cells was significantly decreased in these patients. On the other hand, plasma viscosity and fibrinogen values were in the normal range in both groups and hematocrit was only slightly elevated in patients with angina. Furthermore, there were no changes in rheological parameters during the period of observation (1 week). We can suppose that the hyperviscosity is due, above all, to the decreased red blood cell deformability both in coronary disease patients but also in high-risk subjects. It is probable that red blood cell damage is present before the acute ischemic event, and that is a preexisting cause and not a consequence of it.
A hemophilia B patient, seropositive for HIV antibodies since 1984, came to us in March 1989 with a severe necrotizing lesion of the nose. It was an erythematous lesion and looked like rhinophyma. Microbiological examination of the skin biopsy showed the presence of Cryptococcus neoformans. At the time of the study, the patient was in partial remission after 2 weeks of therapy with fluconazole per os 400 mg/day. He will be treated with the same therapy at maintenance dose (200 mg/day) for a long period.
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